Immune therapies finally working against cancer By MARILYNN MARCHIONE, AP
posted: 4 HOURS 3 MINUTES AGOcomments: 1PrintShareText SizeAAAORLANDO, Fla. -First there was surgery, then chemotherapy and radiation. Now, doctors have overcome 30 years of false starts and found success with a fourth way to fight cancer: using the body's natural defender, the immune system.
The approach is called a cancer vaccine, although it treats the disease rather than prevents it.
At a cancer conference Sunday, researchers said one such vaccine kept a common form of lymphoma from worsening for more than a year. That's huge in this field, where progress is glacial and success with a new treatment is often measured in weeks or even days.
Experimental vaccines against three other cancers &#8212; prostate, the deadly skin disease melanoma and an often fatal childhood tumor called neuroblastoma &#8212; also gave positive results in late-stage testing in recent weeks, after decades of struggles in the lab.
"I don't know what we did differently to make the breakthrough," said Dr. Len Lichtenfeld of the American Cancer Society.

To me, this is great news. I have always felt that chemo and radiation were the wrong answer as killing good cells is never a good thing. But using the immune system to do what it is supposed to do seems to make sense. No cure alls yet, but I am glad to see them pursuing this path.

The team hid cancer killing viruses inside the immune system in order to sneak them into a tumour. Once inside, a study in the journal Cancer Research showed, tens of thousands of viruses were released to kill the cancerous cells. Experts labelled the study "exciting," but human tests are still needed. Using viruses to destroy rapidly growing tumours is an emerging field in cancer therapy, however one of the challenges is getting the viruses deep inside the tumour where they can do the damage. "The problem is penetration," Prof Claire Lewis from the University of Sheffield told the BBC. She leads a team which uses white blood cells as 'Trojan horses' to deliver the viral punch.

'Surfing'

After chemotherapy or radiotherapy is used to treat cancer, there is damage to the tissue. This causes a surge in white blood cells, which swamp the area to help repair the damage. "We're surfing that wave to get as many white blood cells to deliver tumour-busting viruses into the heart of a tumour," said Prof Lewis. Her team takes blood samples and extract macrophages, a part of the immune system which normally attacks foreign invaders. These are mixed with a virus which, just like HIV, avoids being attacked and instead becomes a passenger in the white blood cell. In the study, the mice were injected with the white blood cells two days after a course of chemotherapy ended. At this stage each white blood cell contained just a couple of viruses. However, once the macrophages enter the tumour the virus can replicate. After about 12 hours the white blood cells burst and eject up to 10,000 viruses each - which go on to infect, and kill, the cancerous cells.

Gone

At the end of the 40-day study, all the mice who were given the Trojan treatment were still alive and had no signs of tumours. By comparison, mice given other treatments died and their cancer had spread. Prof Lewis said: "It completely eradicates the tumour and stops it growing back." She said it was a "ground-breaking" concept, but cautioned that many remarkable advances in treating mice failed to have any effect in people. She hopes to begin human trials next year. Dr Emma Smith, from Cancer Research UK, said: "Harnessing the body's own immune system to deliver a deadly virus to tumours is an exciting approach that many scientists are pursuing. "This study shows it has the potential to make chemotherapy and radiotherapy more effective weapons against cancer. She said the research was still at an early stage and tests to show it is safe and effective in humans are still needed.

Dr Kate Holmes, head of research at Prostate Cancer UK, said: "It demonstrates that this innovative method of delivering a tumour-killing virus direct to the cancer site is successful at reducing the development of advanced prostate tumours in mice which have been treated with chemotherapy and radiotherapy. "If this treatment goes on to be successful in human trials, it could mark substantial progress in finding better treatments for men with prostate cancer which has spread to the bone."

Now the question is how to hold onto those gains, and do even better, even as the population gets older and fatter, both risks for developing cancer. "There has been clear progress," said Dr. Otis Brawley of the American Cancer Society, which compiled the annual cancer report with government and cancer advocacy groups. But bad diets, lack of physical activity and obesity together wield "incredible forces against this decline in mortality," Brawley said. He warned that over the next decade, that trio could surpass tobacco as the leading cause of cancer in the U.S.

Overall, deaths from cancer began slowly dropping in the 1990s, and Monday's report shows the trend holding. Among men, cancer death rates dropped by 1.8 percent a year between 2000 and 2009, and by 1.4 percent a year among women. The drops are thanks mostly to gains against some of the leading types - lung, colorectal, breast and prostate cancers - because of treatment advances and better screening. The news isn't all good. Deaths still are rising for certain cancer types including liver, pancreatic and, among men, melanoma, the most serious kind of skin cancer. Preventing cancer is better than treating it, but when it comes to new cases of cancer, the picture is more complicated.

Cancer incidence is dropping slightly among men, by just over half a percent a year, said the report published by the Journal of the National Cancer Institute. Prostate, lung and colorectal cancers all saw declines. But for women, earlier drops have leveled off, the report found. That may be due in part to breast cancer. There were decreases in new breast cancer cases about a decade ago, as many women quit using hormone therapy after menopause. Since then, overall breast cancer incidence has plateaued, and rates have increased among black women.

Another problem area: Oral and anal cancers caused by HPV, the sexually transmitted human papillomavirus, are on the rise among both genders. HPV is better known for causing cervical cancer, and a protective vaccine is available. Government figures show just 32 percent of teen girls have received all three doses, fewer than in Canada, Britain and Australia. The vaccine was recommended for U.S. boys about a year ago. Among children, overall cancer death rates are dropping by 1.8 percent a year, but incidence is continuing to increase by just over half a percent a year. Brawley said it's not clear why.

The animals had melanoma, which can rapidly become resistant to treatments. However, a study in the journal Nature showed tumours also became dependent on the drug to survive. Withdrawing treatment caused tumours to shrink. Experts said the findings were exciting, but still needed testing in people. A team of scientists at the University of California, San Francisco and University Hospital Zurich, in Switzerland, were investigating how melanoma cells became resistant to a drug, vemurafenib. The drug can slow the progress of a tumour in the short-term, but it soon becomes ineffective with deadly consequences.

Addiction

The tumours gain resistance by changing the chemistry of the inside of a cell. However, the researchers showed this process left the cancer cells dependent on the drug - like an addict. When the mice were no longer given the drug, the tumours began to shrink. The scientists used this knowledge to test a new way of prescribing the medication. Instead of giving the drug every day, the mice were given drugs for four weeks and then had a two week "drug holiday" before starting the pattern over again. Efim Guzik, professor of cancer biology at University of California, San Francisco, said: "Remarkably, intermittent dosing with vemurafenib prolonged the lives of mice with drug-resistant melanoma tumours. "By seeking to understand the mechanisms of drug resistance, we have also found a way to enhance the durability of the drug response."

Whether the same effect would be seen in people given the same medication is uncertain. Prof Mark Middleton, director of Cancer Research UK's Experimental Cancer Medicine Centre in Oxford, said: "We still need to test the idea in the clinic, but these results suggest a way in which this important new treatment might be able to increase the benefit to patients and their families. "It also offers the possibility of more cost effective treatment, with fewer side effects, because patients would spend some of the time off vemurafenib."

Vemurafenib targets a mutated protein called BRAF. Prof Richard Marais, from the Paterson Institute for Cancer Research in Manchester, was involved in the discovery of the BRAF fault. He said the findings were "very compelling". "This new study is exciting because it suggests a way to combat the evolution of drug resistance in melanoma patients using the drugs we already have, rather than having to develop new ones. "It will be interesting to see if these lab results are mirrored in clinical trials." Prof Marais said the same effect is possible in other forms of targeted cancer drug treatment.

Sixteen patients given a high dose of the therapy survived for 14.1 months on average, compared to 6.7 months for the 14 who got the low dose. "For the first time in medical history we have shown that a genetically-engineered virus can improve survival of cancer patients," study co-author David Kirn told AFP.

The four-week trial with the vaccine Pexa-Vec or JX-594, reported in the journal Nature Medicine, may hold promise for the treatment of advanced solid tumours. "Despite advances in cancer treatment over the past 30 years with chemotherapy and biologics, the majority of solid tumours remain incurable once they are metastatic (have spread to other organs)," the authors wrote. There was a need for the development of "more potent active immunotherapies", they noted.

Pexa-Vec "is designed to multiply in and subsequently destroy cancer cells, while at the same time making the patients' own immune defence system attack cancer cells also," said Kirn from California-based biotherapy company Jennerex. "The results demonstrated that Pexa-Vec treatment at both doses resulted in a reduction of tumour size and decreased blood flow to tumours," said a Jennerex statement. "The data further demonstrates that Pexa-Vec treatment induced an immune response against the tumour."

Pexa-Vec has been engineered from the vaccinia virus, which has been used as a vaccine for decades, including in the eradication of smallpox. The trial showed Pexa-Vec to be well tolerated both at high and low doses, with flu-like symptoms lasting a day or two in all patients and severe nausea and vomiting in one. The authors said a larger trial has to confirm the results. A follow-up phase with about 120 patients is already underway. Pexa-Vec is also being tested in other types of cancer tumours.

New genetic test for cancer markers...DNA test reveals 80 markers for inherited cancer risk27 March 2013 - More than 80 genetic markers that can increase the risk of developing breast, prostate or ovarian cancer have been found in the largest study of its kind.

The DNA of 200,000 people - half of them with cancer and half without - was compared, revealing an individual's inherited risk of the diseases. British scientists, who led the research, believe it could lead to a DNA screening test within five years. They also hope it will boost knowledge of how the cancers develop. The research was led by scientists at the University of Cambridge and the Institute of Cancer Research (ICR) in London and funded by Cancer Research UK (CRUK) and the Wellcome Trust. The main findings are published in five articles in the journal Nature Genetics. Study author Prof Doug Easton said: "We're on the verge of being able to use our knowledge of these genetic variations to develop test that could complement breast cancer screening and take us a step closer to having an effective prostate cancer screening programme."

Inherited cancer risk

The scientists looked for common genetic variations - known as single nucleotide polymorphisms (Snps) - linked to the three cancers. Each alteration raised the risk of cancer by a small amount. However, a small minority of men with lots of the markers could see their risk of prostate cancer increase more than fourfold and for women the breast cancer risk increase threefold. By contrast, the test can also identify those with a smaller than average risk of developing the cancers. A woman's lifetime risk of breast cancer is one in eight, but among the 1% with lots of these newly identified genetic variations the risk rises to one in two. The test could also help the one in 300 woman who carry a faulty gene known as BRCA1 or BRCA2. Two-thirds of them will develop breast cancer before the age of 80 and 45% who carry BRCA1 will get ovarian cancer.

At present the options to reduce their risks are limited - a double mastectomy or having their ovaries removed. By combining the gene test for BRCA1 and BRCA2 with this extra genetic information, women who have a high number of the newly identified markers could find they have a nearly 100% risk of getting breast cancer. In contrast, those with the protective versions of the genetic changes could see their risk drop to as low as 20%. Dr Antonis Antoniou, CRUK senior fellow at the University of Cambridge, said: "Our research puts us on the verge of being able to give women a much more accurate picture of how likely they are to develop breast or ovarian cancer and would help to guide them about the most appropriate type and time of prevention or monitoring options for them."

New Cancer Research Seen Leading to Better Screening, Potential New Drugs March 27, 2013 &#8212; New research has nearly doubled the number of genetic variations implicated in breast, prostate and ovarian cancer, offering fresh avenues for screening at-risk patients and, potentially, developing better drugs.

The bumper haul of 74 gene changes that can increase risks for the three hormone-related cancers, announced by scientists on Wednesday, is the result of the largest ever study of its kind. It follows an international project to analyse the DNA of more than 200,000 people - half of them with cancer and half from the general population - to find alterations that are more common in individuals with the disease. Although each gene variation increases cancer risk by only a small amount, scientists calculate that the 1 percent of men carrying lots of the alterations could have a 50 percent increased risk of developing prostate cancer. Women with multiple variants could see their risk of breast cancer increase by 30 percent.

DNA double helix is seen in an undated artist's illustration released by the National Human Genome Research Institute

Doug Easton of the University of Cambridge, one of the cancer researchers who led the work, said the batch of new genetic discoveries meant medical experts would be able to develop new cancer screening programmes. This will take time, since more research is needed to develop diagnostic tools. "I would think that within five to 10 years this might be being used commonly, if not in a very widespread population base,'' said Paul Pharoah, also of the University of Cambridge. Initially, the additional screening is likely to be targeted at patients with established cancer risk factors, such as carriers of BRCA gene faults. Women with BRCA faults are known to be at greater risk of developing breast and ovarian cancer.

NEW DRUGS

Ros Eeles of Britain's Institute of Cancer Research, an expert in prostate cancer, said the new findings were the biggest leap forward yet in understanding the genetic basis of the disease. "They allow us, for the first time, to identify men who have a very high risk of developing prostate cancer during their lifetime through inheritance of multiple risk genetic variants,'' she said. In the case of prostate cancer, scientists found 23 new genetic variations - known as single nucleotide polymorphisms, or SNPs - taking the total to 78. Significantly, 16 were linked with the more aggressive forms of the disease. For breast cancer the researchers found 49 new SNPs, more than doubling the number previously identified, and in ovarian cancer the tally was 11. A few of the variations were common to more than one cancer type, suggesting there may be common mechanisms of action that could be targeted by new drugs.

Developing medicines using the insight gained by the latest research will take many years, even assuming that drugmakers can produce compounds that work effectively. Encouragingly, though, companies such as Roche, the market leader in cancer, are getting better at making drugs that apply biochemical brakes'' to tumour cells. The scientists stressed that genes, while important, were just one side of a complex mix of factors leading to cancer. "Lifestyle and environmental risks act in concert with the genetics. It is not one or the other - it is always both together,'' Pharoah told reporters. The new research was published in a series of papers in Nature Genetics, Nature Communications, PLOS Genetics, the American Journal of Human Genetics and Human Molecular Genetics.

Belgian Researchers Discover Way to Block Cancer Metastasis September 18, 2014: WASHINGTON — Cancer remains one of the deadliest diseases, despite many new methods to combat it. Modern medicine has treatments to prevent the growth of primary tumor cells. But most cancer deaths are caused by metastasis, when primary tumor cells change and move to other parts of the body. A team of Belgian scientists says it has found a way to prevent that process.

Metastasis occurs as primary tumor cells leave the tumor, get into the blood stream, pass through the circulatory system, and then find new tissue to colonize. Belgian scientists at a research institute of the Université Catholique de Louvain say they have discovered a way to prevent the metastasis of primary tumors from breast and melanomic cancer cells in mice. "When you have few metastases, this is still manageable for therapy. But when you have a lot of metastases all around your body, you are good for palliative care, it's sad to say so. So what we've found is a treatment able to prevent metastases. Of course, this offers a high hope for patients which are at risk for metastases," said Professor Pierre Sonveaux of the Université Catholique de Louvain.

Cancer specialists say metastasis is a complicated process about which much is still unknown. "For instance, cells have to change their shapes in order to metastasize, and we don't understand basic questions about how cells can change their shape," said the Institute of Cancer Research’s Chris Bakal. The Belgian team led by Sonveaux has found the mechanism by which cells can control changes caused at least in part by free radicals. The free radical involved in the metastacism of tumor cells is superoxide. Tests in mice on melanoma and breast cancer cells showed that administering an antioxidant stopped the production of superoxide. That, in turn, prevented cell changes that would lead to metastasis. "In some of these models, we found 100 percent response. It means that we prevented by 100 percent the dissemination of metastases. When you are a scientist and when you find this, you just fall on the ground. This is a very nice result," said Sonveaux.

The research, published in the journal Cell Reports, has drawn praise from other scientists. Bakal said the findings could lead to the development of a therapy to prevent the spread of metastatic cancer cells by blocking pathways to free radicals. "What it suggests is that by targeting these pathways, these free radical pathways, it could represent a way, a therapeutic avenue, by which to inhibit metastasis, which we weren't necessarily clear of before. So if we lower the amount of free radicals in metastatic cells, it suggests we could prevent metastasis," said Bakal. Belgian researchers say they now want to find out if this strategy can be applied to prevent metastasis of other tumors, such as colon cancer, lung cancer and prostate cancer. The next step would be developing the necessary drugs and starting clinical trials on cancer patients.

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